Plasmacytoid Dendritic Cells In Pulmonary Lymphoid Follicles Of Patients With COPD

Pottelberge, Geert Van; Bracke, Ken; Broeck, Sarah Van den; Reinartz, Susanne M.; Drunen, Cornelis M. van; Wouters, Emiel F.M.; Verleden, Geert M.; Vermassen, Frank; Joos, Guy

doi:10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a3882

Cited by 2 publications

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“…These may include delivery of regulatory homeostatic chemokines and cytokines or interventions that block Treg involvement at ELFs. 65,100 ELFs as perpetuators of inflammation-driven pathology Ectopic lymphoid follicles are associated with various autoimmune and chronic inflammatory diseases including rheumatoid arthritis, 11,101,102 Sj€ ogren syndrome, 103 multiple sclerosis, 104 experimental diabetes, 105 atherosclerosis, 106,107 inflammatory bowel disease 108,109 and chronic obstructive pulmonary disease 110,111 (for a comprehensive review of ELFs in autoimmunity see refs 10,76). In contrast to their roles in infection and cancer, ELFs in chronic inflammatory diseases are primarily associated with disease exacerbation.…”

Section: Elfs As Regulators Of Anti-tumour Immunitymentioning

confidence: 99%

Ectopic lymphoid follicles: inducible centres for generating antigen‐specific immune responses within tissues

2015

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SummaryLymphoid neogenesis is traditionally viewed as a pre‐programmed process that promotes the formation of lymphoid organs during development. Here, the spatial organization of T and B cells in lymph nodes and spleen into discrete structures regulates antigen‐specific responses and adaptive immunity following immune challenge. However, lymphoid neogenesis is also triggered by chronic or persistent inflammation. Here, ectopic (or tertiary) lymphoid organs frequently develop in inflamed tissues as a response to infection, auto‐immunity, transplantation, cancer or environmental irritants. Although these structures affect local immune responses, the contribution of these lymphoid aggregates to the underlining pathology are highly context dependent and can elicit either protective or deleterious outcomes. Here we review the cellular and molecular mechanisms responsible for ectopic lymphoid neogenesis and consider the relevance of these structures in human disease.

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Section: Elfs As Regulators Of Anti-tumour Immunitymentioning

confidence: 99%

Ectopic lymphoid follicles: inducible centres for generating antigen‐specific immune responses within tissues

2015

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“…LFs consist of compact and organized B cell follicles with central FDC networks and surrounded by T cells. LFs have been previously detected in the parenchyma and in bronchial walls of patients with COPD and chronic CS-exposed mice (58)(59)(60). In chronic CS-exposure models, clonal expansion and antigen-induced proliferation in B cell follicles were associated with progressive inflammation and an increase in alveolar airspace enlargement, as a result of local autoantibody production against CS components or other components of the extracellular matrix (61).…”

Section: Discussionmentioning

confidence: 98%

Genetic ablation of histone deacetylase 2 leads to lung cellular senescence and lymphoid follicle formation in COPD/emphysema

et al. 2018

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Histone deacetylase 2 (HDAC2), a critical determinant of chromatin remodeling, is reduced as a consequence of oxidative stress-mediated DNA damage and impaired repair. Cigarette smoke (CS) exposure causes DNA damage and cellular senescence. However, no information is available on the role of HDAC2 in CS-induced DNA damage, stress-induced premature senescence (SIPS), and senescence-associated secretory phenotype (SASP) during the pathogenesis of chronic obstructive pulmonary disease (COPD)/emphysema. We hypothesized that CS causes persistent DNA damage and cellular senescence via HDAC2-dependent mechanisms. We used HDAC2 global knockout (KO) and HDAC2 lung epithelial cell-specific KO [Clara cell-specific HDAC2 deletion (HDAC2 CreCC10)] mice to determine whether HDAC2 is a major player in CS-induced oxidative stress, SIPS, and SASP. HDAC2 KO mice exposed to CS show exaggerated DNA damage, inflammatory response, and decline in lung function leading to airspace enlargement. Chronic CS exposure augments lung senescence-associated β-galactosidase activity in HDAC2 KO, but not in HDAC2 CreCC10 mice. HDAC2 lung epithelial cell-specific KO did not further augment CS-induced inflammatory response and airspace enlargement but instead caused an increase in lymphoid aggregate formation. Our study reveals that HDAC2 is a key player regulating CS-induced DNA damage, inflammatory response, and cellular senescence leading to COPD/emphysema.-Sundar, I. K., Rashid, K., Gerloff, J., Rangel-Moreno, J., Li, D., Rahman, I. Genetic ablation of histone deacetylase 2 leads to lung cellular senescence and lymphoid follicle formation in COPD/emphysema.

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Plasmacytoid Dendritic Cells In Pulmonary Lymphoid Follicles Of Patients With COPD

Cited by 2 publications

References 0 publications

Ectopic lymphoid follicles: inducible centres for generating antigen‐specific immune responses within tissues

Ectopic lymphoid follicles: inducible centres for generating antigen‐specific immune responses within tissues

Genetic ablation of histone deacetylase 2 leads to lung cellular senescence and lymphoid follicle formation in COPD/emphysema

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